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Image by Andre E.X. Brown
Researchers say they have determined how procoagulant platelets develop.
One of the mysteries in the field of thrombosis and hemostasis is how platelets are divided into two kinds when activated—“ordinary” platelets capable of aggregation and “super-activated,” procoagulant platelets.
The new study suggests that, to become super-activated, platelets must die. And the platelets need mitochondria to commit suicide.
Researchers were able to show how this programmed death—mitochondrial necrosis—follows a chain of events that lead to the platelets’ transition to a super-activated state.
“It was not clear before how a platelet makes the decision of what type to become,” said study author Mikhail Panteleev, of Lomonosov Moscow State University in Russia.
“We have deciphered the sequence of events: how the signal goes within the platelet and how the cell decides to die.”
Panteleev and his colleagues described these events in the Journal of Thrombosis and Haemostasis.
The team noted that platelets have many activators, but the chief among them are collagen, ADP, and thrombin.
Platelets detect different concentrations of an activator and respond with a varying frequency of calcium impulses in the cytoplasm.
The platelets’ mitochondria absorb and store the calcium, and when its concentration exceeds the critical level, the process of mitochondrial necrosis starts.
Calcium and reactive oxygen species are released from mitochondria, ATPases begin to destroy ATP instead of synthesizing it, the cell cytoskeleton collapses, and the platelets greatly increase in size.
As a result, at the outer membrane of the enlarged platelets, a lipid called phosphatidylserine appears, which is responsible for rapid blood clotting. And all this happens in seconds. 
Image by Andre E.X. Brown
Researchers say they have determined how procoagulant platelets develop.
One of the mysteries in the field of thrombosis and hemostasis is how platelets are divided into two kinds when activated—“ordinary” platelets capable of aggregation and “super-activated,” procoagulant platelets.
The new study suggests that, to become super-activated, platelets must die. And the platelets need mitochondria to commit suicide.
Researchers were able to show how this programmed death—mitochondrial necrosis—follows a chain of events that lead to the platelets’ transition to a super-activated state.
“It was not clear before how a platelet makes the decision of what type to become,” said study author Mikhail Panteleev, of Lomonosov Moscow State University in Russia.
“We have deciphered the sequence of events: how the signal goes within the platelet and how the cell decides to die.”
Panteleev and his colleagues described these events in the Journal of Thrombosis and Haemostasis.
The team noted that platelets have many activators, but the chief among them are collagen, ADP, and thrombin.
Platelets detect different concentrations of an activator and respond with a varying frequency of calcium impulses in the cytoplasm.
The platelets’ mitochondria absorb and store the calcium, and when its concentration exceeds the critical level, the process of mitochondrial necrosis starts.
Calcium and reactive oxygen species are released from mitochondria, ATPases begin to destroy ATP instead of synthesizing it, the cell cytoskeleton collapses, and the platelets greatly increase in size.
As a result, at the outer membrane of the enlarged platelets, a lipid called phosphatidylserine appears, which is responsible for rapid blood clotting. And all this happens in seconds.
Image by Andre E.X. Brown
Researchers say they have determined how procoagulant platelets develop.
One of the mysteries in the field of thrombosis and hemostasis is how platelets are divided into two kinds when activated—“ordinary” platelets capable of aggregation and “super-activated,” procoagulant platelets.
The new study suggests that, to become super-activated, platelets must die. And the platelets need mitochondria to commit suicide.
Researchers were able to show how this programmed death—mitochondrial necrosis—follows a chain of events that lead to the platelets’ transition to a super-activated state.
“It was not clear before how a platelet makes the decision of what type to become,” said study author Mikhail Panteleev, of Lomonosov Moscow State University in Russia.
“We have deciphered the sequence of events: how the signal goes within the platelet and how the cell decides to die.”
Panteleev and his colleagues described these events in the Journal of Thrombosis and Haemostasis.
The team noted that platelets have many activators, but the chief among them are collagen, ADP, and thrombin.
Platelets detect different concentrations of an activator and respond with a varying frequency of calcium impulses in the cytoplasm.
The platelets’ mitochondria absorb and store the calcium, and when its concentration exceeds the critical level, the process of mitochondrial necrosis starts.
Calcium and reactive oxygen species are released from mitochondria, ATPases begin to destroy ATP instead of synthesizing it, the cell cytoskeleton collapses, and the platelets greatly increase in size.
As a result, at the outer membrane of the enlarged platelets, a lipid called phosphatidylserine appears, which is responsible for rapid blood clotting. And all this happens in seconds.